CD58 expression of liver tissue in patients with chronic hepatitis B virus infection

Wang, Ping; Qi, Bao-tai; Chen, Ping; He, Linjing; Li, Jie; Ji, Yibing; Xie, Ming

doi:10.1097/00029330-200803020-00018

Cited by 3 publications

(2 citation statements)

References 22 publications

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“…Regarding cell adhesion molecules (CAMs), undifferentiated ADHLSCs, differentiated ADHLSCs, and hepatocytes are negative for CD31 (with anti-inflammatory properties in the liver) [ 23 ], CD58 (proposed to augment cell mediated immunity against hepatitis B virus and thus leading to hepatocyte destruction) [ 24 ], CD62e, CD102 (involved in recruitment of lymphocytes to the liver) [ 25 ], and CD146 (although poorly characterized but described to be involved in angiogenesis) [ 26 ]. However, all cells are positive to CD29 (essential for hepatocyte survival) [ 27 ], CD49e, and CD166 (playing an antiapoptotic role for liver cells) [ 28 ] regardless of presence or absence of inflammatory signals.…”

Section: Discussionmentioning

confidence: 99%

Immunoprofiling of Adult-Derived Human Liver Stem/Progenitor Cells: Impact of Hepatogenic Differentiation and Inflammation

El-Kehdy

Sargiacomo

Fayyad‐Kazan

et al. 2017

Stem Cells International

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Adult-derived human liver stem/progenitor cells (ADHLSCs) are, nowadays, developed as therapeutic medicinal product for the treatment of liver defects. In this study, the impact of hepatogenic differentiation and inflammation priming on the ADHLSCs' immune profile was assessed in vitro and compared to that of mature hepatocytes. The constitutive immunological profile of ADHLSCs was greatly different from that of hepatocytes. Differences in the expression of the stromal markers CD90 and CD105, adhesion molecules CD44 and CD49e, immunoregulatory molecules CD73 and HO-1, and NK ligands CD112 and CD155 were noted. While they globally preserved their immunological profile in comparison to undifferentiated counterparts, differentiated ADHLSCs showed a significant downregulation of CD200 expression as in hepatocytes. This was mainly induced by signals issued from EGF and OSM. On the other hand, the impact of inflammation was quite similar for all studied cell populations with an increased expression level of CD54 and CD106 and induction of that of CD40 and CD274. In conclusion, our immune profiling study suggests CD200 as a key factor in regulating the immunobiology of differentiated ADHLSCs. A better understanding of the molecular and physiological events related to such marker could help in designing the optimal conditions for an efficient therapeutic use of ADHLSCs.

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Section: Discussionmentioning

confidence: 99%

Immunoprofiling of Adult-Derived Human Liver Stem/Progenitor Cells: Impact of Hepatogenic Differentiation and Inflammation

El-Kehdy

Sargiacomo

Fayyad‐Kazan

et al. 2017

Stem Cells International

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“…Although studies on CD2 in MASLD are limited, enhanced CD58 expression has been found to correlate with the degree of hepatocellular injury in patients with chronic HBV infection. This could be attributed to its binding to CD2 , which accelerates the activation of T and NK cells, thus intensifying the cellular immune response to eliminate HBV and potentially leading to liver tissue damage ( 50 ). Moreover, in hepatitis C, increased CD2-associated proteins have been demonstrated to influence lipid metabolism through the IRS1-Akt-AMPK-HSL pathway, causing deactivation of hormone-sensitive lipase and consequent augmentation of lipid droplet accumulation, ultimately promoting steatosis ( 51 ).…”

Section: Discussionmentioning

confidence: 99%

Identification and validation of hub genes expressed in ulcerative colitis with metabolic dysfunction-associated steatotic liver disease

Liu,

Li,

Tian

et al. 2024

Front. Immunol.

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ObjectiveUlcerative colitis (UC) and metabolic dysfunction-associated steatotic liver disease (MASLD) are closely intertwined; however, the precise molecular mechanisms governing their coexistence remain unclear.MethodsWe obtained UC (GSE75214) and MASLD (GSE151158) datasets from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were acquired by the ‘edgeR’ and ‘limma’ packages of R. We then performed functional enrichment analysis of common DEGs. Hub genes were selected using the cytoHubba plugin and validated using GSE87466 for UC and GSE33814 for MASLD. Immunohistochemistry was employed to validate the hub genes’ expression in clinical samples. Immune infiltration and gene set enrichment analyses of the hub genes were performed. Finally, we estimated the Spearman’s correlation coefficients for the clinical correlation of the core genes.ResultsWithin a cohort of 26 differentially regulated genes in both UC and MASLD, pathways involving cytokine-mediated signaling, cell chemotaxis, and leukocyte migration were enriched. After further validation, CXCR4, THY1, CCL20, and CD2 were identified as the hub genes. Analysis of immune infiltration patterns highlighted an association between elevated pivotal gene expression and M1 macrophage activation. Immunohistochemical staining revealed widespread expression of pivotal genes in UC- and MASLD-affected tissues. Furthermore, significant correlations were observed between the increased expression of hub genes and biochemical markers, such as albumin and prothrombin time.ConclusionThis bioinformatics analysis highlights CXCR4, THY1, CCL20, and CD2 as crucial genes involved in the co-occurrence of UC and MASLD, providing insights into the underlying mechanisms of these two conditions.

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Structure-based identification of inhibitors disrupting the CD2–CD58 interactions

Tripathi

Leherte

Vercauteren

et al. 2021

J Comput Aided Mol Des

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CD58 expression of liver tissue in patients with chronic hepatitis B virus infection

Cited by 3 publications

References 22 publications

Immunoprofiling of Adult-Derived Human Liver Stem/Progenitor Cells: Impact of Hepatogenic Differentiation and Inflammation

Immunoprofiling of Adult-Derived Human Liver Stem/Progenitor Cells: Impact of Hepatogenic Differentiation and Inflammation

Identification and validation of hub genes expressed in ulcerative colitis with metabolic dysfunction-associated steatotic liver disease

Structure-based identification of inhibitors disrupting the CD2–CD58 interactions

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